The essential fatty acids (EFA), linoleate (18:2n6) and linolenate (18:3n3), are desaturated and elongated to arachidonate (20:4n6) and docosahexaenoate (22:6n3), respectively. A stable isotope gas chromatography-mass spectrometry (GC-MS) method is being used to examine these processes in vivo. Studies in mice, rats, cats, rhesus monkeys and humans have suggested that all mammals have elongation and desaturation capability and that their products may be monitored in the blood. In general, ethanol consumption lowers the levels of 20:4n6 and 22:6n3 in the blood cells and livers of animals. We have shown that the mechanisms underlying the disruption of the essential fatty acid levels in these tissues are, in part, due to the inhibition of the elongation/desaturation of 18-carbon essential fatty acids by alcohol. A study in felines given alcohol for six months showed marked reductions of 20:4n6 and 22:6n3 in the liver and blood compared to controls. In the brain and retina the levels of 22:6n3 decreased, however, 20:4n6 levels remained unchanged. In a rhesus monkey study where the diet contained low but adequate amounts of essential fatty acids and minimal levels of antioxidants, 12 months of alcohol exposure led to sharp declines in the level of 22L6n3 in the liver and plasma. The level of 20:4n6 in the plasma also decreased by about 50%. The levels of 22:6n3 in the brain and retina of an alcohol exposed monkey were much lower relative to chow-fed animals. It is suggested, therefore, that chronic alcohol exposure causes an EFA deficiency in animals which leads to lower amounts of 22:6n3 in the nervous system. A related study in felines indicated that the maintenance of neural long chain polyunsaturates is necessary for the proper development of retinal function.